Journal: Oncogenesis

Article Title: Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway

doi: 10.1038/oncsis.2017.84

Figure Lengend Snippet: Colorectal carcinoma CM enhanced the migration, invasion, tube formation and Dil-Ac-LDL uptake abilities of NECs. ( a ) NECs monolayer was wounded and induced by SW620, HT-29 or HCT116 CM. Photographs were taken after induction for 0, 24 and 48 h (scale bar 40 μm). ( b ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h. The number of invaded cells was counted in three random fields. Representative images of invaded cells were shown (scale bar 40 μm). ( c ) Formation tubes in each group were photographed. The number of tubes per field was counted in three random fields (scale bar 20 μm). ( d ) Representative images showed the Dil-Ac-LDL uptake ability of NECs and quantification of the relative Dil-Ac-LDL uptake (scale bar 40 μm). Data are presented as mean±s.d. from three independent experiments. *** P <0.001.

Article Snippet: The human colorectal cancer cell lines SW620, HT-29 and HCT116 were obtained from Nanjing Keygen Biotech Corp. (Nanjing, China), and cultured in RPMI-1640 (Biological Industries, Kibbutz Beit Haemek, Israel) medium with 10% fetal bovine serum.

Techniques: Migration

Journal: Oncogenesis

Article Title: Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway

doi: 10.1038/oncsis.2017.84

Figure Lengend Snippet: Colorectal carcinoma CM promoted the transition of NECs toward TECs. ( a ) Immunohistochemical staining for TECs markers (TEM1, TEM8 and VEGFR2) in colorectal carcinoma and peri-carcinoma tissue (scale bar 20 μm). ( b ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h. The relative mRNA levels of TECs markers were determined by qRT–PCR. ( c , d ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h, the protein levels of TECs markers were detected by western blot ( c ) and immunofluorescence ( d ). Data are presented as mean±s.d. from three independent experiments. ** P <0.01, *** P <0.001.

Article Snippet: The human colorectal cancer cell lines SW620, HT-29 and HCT116 were obtained from Nanjing Keygen Biotech Corp. (Nanjing, China), and cultured in RPMI-1640 (Biological Industries, Kibbutz Beit Haemek, Israel) medium with 10% fetal bovine serum.

Techniques: Immunohistochemical staining, Staining, Quantitative RT-PCR, Western Blot, Immunofluorescence

Journal: Oncogenesis

Article Title: Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway

doi: 10.1038/oncsis.2017.84

Figure Lengend Snippet: JAK/STAT3 signaling pathway was activated during the transition of NECs toward TECs induced by colorectal carcinoma CM. ( a ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h. The relative mRNA levels of JAK and STAT3 were measured by qRT–PCR. ( b , c ) The expression level of indicated protein was detected by western blot ( b ) and immunofluoresence (scale bar 50 μm) ( c ). Data are expressed as mean±s.d. from three independent experiments. * P <0.05, ** P <0.01, *** P <0.001.

Article Snippet: The human colorectal cancer cell lines SW620, HT-29 and HCT116 were obtained from Nanjing Keygen Biotech Corp. (Nanjing, China), and cultured in RPMI-1640 (Biological Industries, Kibbutz Beit Haemek, Israel) medium with 10% fetal bovine serum.

Techniques: Quantitative RT-PCR, Expressing, Western Blot

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Antitumor effect in LIM1215(A) xenografts by treatment received. (A and B) assessed by average tumor volume and (C) relative growth rate. Arrowheads indicate dosing. Arrows indicate sample harvesting. Data represent mean ± SE. ( n = 3–7. * P < .05). B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Outcome of immunohistochemistry for Ki-67 in LIM1215(B) xenograft sections. (A) Using vehicle control, (B) panitumumab-bevacizumab, (C) bevacizumab-panitumumab, and (D) bevacizumab-bevacizumab. (E) Proportion of Ki-67-positive cells in all treatment groups. Sections were IHC stained for Ki-67 (brown) and counterstained with hematoxylin (purple). Representative images of the sections are shown. Data in the graph represent the mean ± SE ( n = 6–8). ** P < .01. B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Immunohistochemistry, Control, Staining

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Levels of Phosphorylated Growth Factor Receptors in LIM1215(A) Xenografts Treated with PB, BP, and BB Relative to Vehicle Control

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Phospho-proteomics, Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Results of western blotting in LIM1215(B) xenografts. (A) EPHA2 and pEPHA2 with panitumumab-bevacizumab compared with bevacizumab-panitumumab. (B) EPHA2 and pEPHA2 with panitumumab-bevacizumab compared with bevacizumab-bevacizumab. (C) Phosphorylation of EPHA2 for panitumumab-bevacizumab compared with bevacizumab-panitumumab and (D) compared with bevacizumab-bevacizumab. (E) RSK and pRSK with panitumumab-bevacizumab compared with bevacizumab-panitumumab and (F) RSK and pRSK with panitumumab-bevacizumab compared with bevacizumab-bevacizumab. (G) Phosphorylation of RSK for panitumumab-bevacizumab compared with bevacizumab-panitumumab and (H) compared with bevacizumab-bevacizumab. Data represent mean ± SD ( n = 8). ** P < .01, *** P < .001. B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Western Blot, Phospho-proteomics, Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Enrichment Analysis of LIM1215(A) Xenografts Treated with Bevacizumab-Bevacizumab Compared with Vehicle Control (all Canonical Pathways, P < .001)

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Control, Activation Assay, Inhibition

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Relative expression of (A–H) lipogenic ( FASN, HMGCR, MVD, LSS ) and (I–L) hypoxia-related ( CA9, TGFBI ) genes in LIM1215(B) xenograft tumors. Expression relative to vehicle control with first-line treatment is shown in (A–D) and (I–J), and with sequential treatment in (E–H) and (K–L). Data represent mean ± SD ( n = 8). * P < .05, ** P < .01. B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Expressing, Control

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Analysis of mutational burden in a panel of 64 CRC cell lines. Mutational characterization and comparison of SNVs and frameshifts among MSS (46 samples), MSI (12 samples), and POLE mutated (6 samples) of CRC models. a The distribution of SNVs per Mb of coding DNA at time 0 is shown for each cell line. b The number of frameshift mutations at time 0 is shown for each cell line. c The number of SNVs per each group is shown (“MSS” refers to MSS cells without POLE mutations; “MSI” includes MSI cells, as well as the SNU1040 cell line which is both MSI and POLE mutated; “POLE” includes only MSS cell lines carrying a POLE mutation). d The number of frameshifts per group is shown. The center line of each box plot indicates the median. p < 0.0001

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: Comparison, Mutagenesis

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: In vitro evolution of mutational landscape in 45 CRC cell lines. Mutational characterization of CRC cells after 90 days of culture (T90 ) in vitro. a Bar charts show the number of novel alterations (SNVs and frameshifts) acquired at T90 (not present at T0) for each cell line. b The number of predicted neoantigens (see the “ ” section) is shown. Each bar represents putative neoepitopes derived from SNVs and frameshifts

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: In Vitro, Immunopeptidomics, Derivative Assay

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Lost and gained mutations across evolving CRC cell lines. For each CRC model, the allelic frequency of SNVs at T0 and T90 are shown. Mutations were called against the reference genome (hg38) with allelic frequency > 1. The y -axis reports all the mutations found in each cell line, whereas the time points data are reported on x -axis

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques:

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Mutational signatures associated with alterations emerging during in vitro or in vivo CRC propagation. Analysis of 30 validated cancer-associated mutational signatures in hypermutated/rapidly evolving CRC cell lines. Signatures associated to MMR-deficient (6, 15, 20, 26), POLE -dependent (10), and MUTYH -associated polyposis (18) are highlighted. Analysis and clustering were performed as reported in the “Methods” section. a Heatmap of signature contributions during replication of CRC cells in vitro by analyzing alterations acquired at T90. b Heatmap of signature contributions during replication of the CRC cells in vivo by comparing xenograft tumors to the corresponding cells at T0 (see the “ ” section for detailed information)

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: In Vitro, In Vivo

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Analysis of cell ploidy in a panel of 64 CRC cell lines. Heatmap showing distribution of ploidy for every segmented region in each cell line. Samples are sorted from most to less mutated as reported in Fig. . The percentage (ploidy) is calculated as described in detail in the “Methods” section

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques:

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Transcriptional analysis of CRC cell lines. Differential expression analysis between hypermutated and non-hypermutated cells. a 183 unique genes differentially expressed between hypermutated (MSI/ POLE ) versus non-hypermutated CRC cells (MSS). Log2 expression values along with the mean change in expression are shown. b Pathway analysis of genes differentially expressed between hypermutated versus non-hypermutated CRC cells using g:Profiler application (see the “ ” section)

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: Quantitative Proteomics, Expressing

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Beta2 microglobulin (B2M) expression is downregulated in EVOLVING-CRC. Transcriptional and protein levels of the B2M gene. a Genes differentially expressed in EVOLVING-CRC relative to STABLE-CRC with a significant p value ( p < 0.05). b Waterfall chart showing B2M expression at RNA level across a panel of 45 CRC cell lines. c Western blot analysis of B2M expression. In gray are highlighted samples for which T90 sequencing were not available. Blots were reprobed with anti-HSP90 antibody to confirm equal loading. d B2M gene alterations on 64 CRC cell lines at T0 (upper panel) and codon affected (lower panel)

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: Expressing, Western Blot, Sequencing

Journal: Journal of Cancer

Article Title: Integrated Multi-omics Analyses Identify CDCA5 as a Novel Biomarker Associated with Alternative Splicing, Tumor Microenvironment, and Cell Proliferation in Colon Cancer Via Pan-cancer Analysis

doi: 10.7150/jca.91082

Figure Lengend Snippet: Correlation between CDCA5 and TME of colorectal cancer with TISCH database. (A) Correlation of CDCA5 with TME in CRC. (B, C) The annotation and distribution of the immune cell types in CRC GSE136394 and CRC GSE13955. The proportion of CDCA5 in different immune cell types in CRC GSE136394 dataset (D, E) and CRC GSE13955 dataset (F, G).

Article Snippet: The human colorectal cancer cell line DLD1 was purchased from Procell Life Science& Technology Co., Ltd (Wuhan,China), which was cultured in DMEM supplemented with 10% heat‐inactivated fetal bovine serum (FBS) (Sijiqing Biologic, Hangzhou, China) and was incubated at 37 ̊C in a humid incubator with air containing 5% CO2.

Techniques:

Journal: Journal of Cancer

Article Title: Integrated Multi-omics Analyses Identify CDCA5 as a Novel Biomarker Associated with Alternative Splicing, Tumor Microenvironment, and Cell Proliferation in Colon Cancer Via Pan-cancer Analysis

doi: 10.7150/jca.91082

Figure Lengend Snippet: Effect of CDCA5 silencing on DLD1 cell proliferation, apoptosis, migration and clone formation abilities. (A) mRNA level of CDCA5 after Si-CDCA5 transfection. (B) The viability of DLD1 cells after Si-CDCA5 transfection. (C) Cell clone formation after CDCA5 knockdown. (D) Cell proliferation after CDCA5 knockdown. (E) CDCA5-siRNA reduced the migration of colon cancer cells. (F) CDCA5-siRNA reduced the invasion of colon cancer cells. (G) Cell apoptosis after CDCA5 knockdown. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.001.

Article Snippet: The human colorectal cancer cell line DLD1 was purchased from Procell Life Science& Technology Co., Ltd (Wuhan,China), which was cultured in DMEM supplemented with 10% heat‐inactivated fetal bovine serum (FBS) (Sijiqing Biologic, Hangzhou, China) and was incubated at 37 ̊C in a humid incubator with air containing 5% CO2.

Techniques: Migration, Transfection, Knockdown

Journal: Nutrients

Article Title: Docosahexaenoic Acid Coordinating with Sodium Selenite Promotes Paraptosis in Colorectal Cancer Cells by Disrupting the Redox Homeostasis and Activating the MAPK Pathway

doi: 10.3390/nu16111737

Figure Lengend Snippet: The SDCT could induce cell death in CRC cells. ( A , B ) SW620 and RKO cells were exposed to sodium selenite for 24 h and then the cell viability was determined by the CCK8 assay, as described in the . ( C , D ) SW620 and RKO cells were exposed to DHA for 24 h, and then the cell viability was determined by the CCK8 assay. ( E – H ) SW620 and RKO cells were exposed to sodium selenite and DHA for 24 h, and then the cell viability was determined by the CCK8 assay. The dose–response matrix and synergy score were determined by SynergyFinder 2.0. ( I ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h and subjected to Calcein-AM/PI staining (Calcein AM: live cells; PI: dead cells). Scale bar: 400 µm. The representative images are shown. The corresponding quantitative histograms from three independent experiments were shown (The values represent the mean ± SD, n = 3. Two-tailed unpaired Student’s t -test. ns: not significant; ** p < 0.01).

Article Snippet: The human CRC cell line SW620 (Rosetta Stone Biotechnology, Jinan, China) was cultured in RPMI 1640 medium (Gibco, Carlsbad, CA, USA).

Techniques: CCK-8 Assay, Staining, Two Tailed Test

Journal: Nutrients

Article Title: Docosahexaenoic Acid Coordinating with Sodium Selenite Promotes Paraptosis in Colorectal Cancer Cells by Disrupting the Redox Homeostasis and Activating the MAPK Pathway

doi: 10.3390/nu16111737

Figure Lengend Snippet: DHA remodels the redox state within cancer cells. ( A – C ) SW620 cells were exposed to DHA for 24 h, and the GSH/GSSG ratio was determined by the methods described in the . ( D ) SW620 cells were exposed to DHA for 24 h, and MDA was determined by the methods described in the . ( E , F ) Assessment of indicated protein levels using Western blotting in SW620 cells exposed to DHA. The corresponding quantitative histograms from three independent experiments were shown (The values represented the mean ± SD, n = 3. Two-tailed unpaired Student’s t -test or one-way ANOVA. ns: not significant; * p < 0.05; ** p < 0.01; **** p < 0.0001).

Article Snippet: The human CRC cell line SW620 (Rosetta Stone Biotechnology, Jinan, China) was cultured in RPMI 1640 medium (Gibco, Carlsbad, CA, USA).

Techniques: Western Blot, Two Tailed Test

Journal: Nutrients

Article Title: Docosahexaenoic Acid Coordinating with Sodium Selenite Promotes Paraptosis in Colorectal Cancer Cells by Disrupting the Redox Homeostasis and Activating the MAPK Pathway

doi: 10.3390/nu16111737

Figure Lengend Snippet: The SDCT disrupts redox homeostasis. ( A , B ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h, and the GSH/GSSG ratio was determined. ( C ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h, and MDA was determined. ( D ) Assessment of indicated protein levels using Western blotting in SW620 cells exposed to 1.5 µM sodium selenite and 25 µM DHA for 24 h. ( E , F ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA for 12 h, and the intracellular ROS level was measured by flow cytometry and a fluorescent microscope. Scale bar: 100 µm. ( G ) The viability of SW620 cells exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h with a pretreatment of 5 mM NAC (3 h). The representative images and the corresponding quantitative histograms from three independent experiments were shown (The values represent the mean ± SD, n = 3. Two- tailed unpaired Student’s t -test. * p < 0.05; *** p < 0.001; **** p < 0.0001 versus control).

Article Snippet: The human CRC cell line SW620 (Rosetta Stone Biotechnology, Jinan, China) was cultured in RPMI 1640 medium (Gibco, Carlsbad, CA, USA).

Techniques: Western Blot, Flow Cytometry, Microscopy, Two Tailed Test, Control

Journal: Nutrients

Article Title: Docosahexaenoic Acid Coordinating with Sodium Selenite Promotes Paraptosis in Colorectal Cancer Cells by Disrupting the Redox Homeostasis and Activating the MAPK Pathway

doi: 10.3390/nu16111737

Figure Lengend Snippet: The SDCT activates MAPKs and induces paraptosis. ( A ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h and observed by light microscopy. The arrows in red indicate cytoplasmic vacuoles. Scale bar: 100 µm. ( B ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA for 12 h and observed by transmission electron microscopy. The L in red indicates lysosomes. The V in red indicates cytoplasmic vacuoles. The N in red indicates a cell nucleus. Scale bar: 2 µm. ( C ) The viability of SW620 cells exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h with a pretreatment of CHX (2 h). ( D ) Assessment of indicated protein levels using Western blotting in SW620 cells exposed to 11.5 µM sodium selenite and 25 µM DHA for 24 h. The representative images and the corresponding quantitative histograms from three independent experiments were shown. (The values represented the mean ± SD, n = 3. Two-tailed unpaired Student’s t -test. *** p < 0.001 versus control).

Article Snippet: The human CRC cell line SW620 (Rosetta Stone Biotechnology, Jinan, China) was cultured in RPMI 1640 medium (Gibco, Carlsbad, CA, USA).

Techniques: Light Microscopy, Transmission Assay, Electron Microscopy, Western Blot, Two Tailed Test, Control

Journal: Nutrients

Article Title: Docosahexaenoic Acid Coordinating with Sodium Selenite Promotes Paraptosis in Colorectal Cancer Cells by Disrupting the Redox Homeostasis and Activating the MAPK Pathway

doi: 10.3390/nu16111737

Figure Lengend Snippet: The redox state dynamically activates the MAPK system. ( A ) Assessment of indicated protein levels and quantitative analysis using Western blotting in SW620 cells exposed to 11.5 µM sodium selenite and 25 µM DHA. ( B – D ) SW620 cells were exposed to 11.5 µM sodium selenite and 25 µM DHA, and the GSH/GSSG ratio was determined by the methods described in the . ( E ) Assessment of indicated protein levels and quantitative analysis using Western blotting in SW620 cells exposed to 11.5 µM sodium selenite and 25 µM DHA. ( F ) Model of cell paraptosis induced by a combination of sodium selenite and DHA. The combined intervention produces excess ROS, inhibits Nrf2/HO-1, destroys redox homeostasis, and finally activates ERK1/2, inducing the paraptosis of CRC cells. The corresponding quantitative histograms from three independent experiments were shown (The values represented the mean ± SD, n=3. One-way ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 versus the control).

Article Snippet: The human CRC cell line SW620 (Rosetta Stone Biotechnology, Jinan, China) was cultured in RPMI 1640 medium (Gibco, Carlsbad, CA, USA).

Techniques: Western Blot, Control